Next Article in Journal
Loss of HuD Sensitizes Neuroblastoma Cells to Palmitate-Driven Stress-Induced Premature Senescence via PPARα Downregulation and FAO Impairment
Previous Article in Journal
Disruption of Cell-Adhesion Signaling Resolves Unwanted Progenitor Specification in Stem Cell-Derived α and β Cell Grafts
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target

1
Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul 02447, Republic of Korea
2
Biomedical Science Institute, Kyung Hee University, Seoul 02447, Republic of Korea
3
Department of Biomedical Science, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea
*
Authors to whom correspondence should be addressed.
Cells 2026, 15(4), 315; https://doi.org/10.3390/cells15040315
Submission received: 7 January 2026 / Revised: 2 February 2026 / Accepted: 6 February 2026 / Published: 7 February 2026
(This article belongs to the Special Issue Lipoprotein and Cardiovascular Diseases Therapy)

Abstract

Lipoprotein(a) [Lp(a)] is a causal, genetically determined risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis (CAVS). Although elevated Lp(a) affects approximately 20% of the global population, specific pharmacological options have long been unavailable, leaving a major gap in residual risk management. This review synthesizes current understanding of Lp(a) molecular architecture, genetics, and metabolism, and integrates mechanistic evidence linking Lp(a) to pro-atherogenic, pro-inflammatory, and pro-thrombotic pathways. We summarize epidemiological and genetic data associating Lp(a) with a broad spectrum of cardiovascular outcomes and discuss current clinical guidelines on screening and risk stratification. Furthermore, we provide an up-to-date overview of the emerging therapeutic landscape, including RNA-targeted therapies and novel oral small molecules. With pivotal phase 3 outcome trials nearing completion, the field is transitioning from viewing Lp(a) as an untreatable biomarker to an actionable therapeutic target, with important implications for precision cardiovascular prevention.
Keywords: Lipoprotein(a); Apolipoprotein(a); atherosclerotic cardiovascular disease; calcific aortic valve stenosis Lipoprotein(a); Apolipoprotein(a); atherosclerotic cardiovascular disease; calcific aortic valve stenosis

Share and Cite

MDPI and ACS Style

Yun, H.R.; Singh, M.K.; Han, S.; Ranbhise, J.S.; Ha, J.; Kim, S.S.; Kang, I. Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target. Cells 2026, 15, 315. https://doi.org/10.3390/cells15040315

AMA Style

Yun HR, Singh MK, Han S, Ranbhise JS, Ha J, Kim SS, Kang I. Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target. Cells. 2026; 15(4):315. https://doi.org/10.3390/cells15040315

Chicago/Turabian Style

Yun, Hyeong Rok, Manish Kumar Singh, Sunhee Han, Jyotsna S. Ranbhise, Joohun Ha, Sung Soo Kim, and Insug Kang. 2026. "Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target" Cells 15, no. 4: 315. https://doi.org/10.3390/cells15040315

APA Style

Yun, H. R., Singh, M. K., Han, S., Ranbhise, J. S., Ha, J., Kim, S. S., & Kang, I. (2026). Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target. Cells, 15(4), 315. https://doi.org/10.3390/cells15040315

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop